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Behavioral Tagging: A Translation of the Synaptic Tagging and Capture Hypothesis.

Moncada D, Ballarini F, Viola H - Neural Plast. (2015)

Bottom Line: BT explains how weak events, only capable of inducing transient forms of memories, can result in lasting memories when occurring close in time with other behaviorally relevant experiences that provide proteins.In this review, we detail the findings supporting the existence of BT process in rodents, leading to the consolidation, persistence, and interference of a memory.We focus on the molecular machinery taking place in these processes and describe the experimental data supporting the BT in humans.

View Article: PubMed Central - PubMed

Affiliation: Instituto de Biologia Celular y Neurociencias "Dr. Eduardo De Robertis", Facultad de Medicina, Universidad de Buenos Aires, C1121ABG Buenos Aires, Argentina.

ABSTRACT
Similar molecular machinery is activated in neurons following an electrical stimulus that induces synaptic changes and after learning sessions that trigger memory formation. Then, to achieve perdurability of these processes protein synthesis is required for the reinforcement of the changes induced in the network. The synaptic tagging and capture theory provided a strong framework to explain synaptic specificity and persistence of electrophysiological induced plastic changes. Ten years later, the behavioral tagging hypothesis (BT) made use of the same argument, applying it to learning and memory models. The hypothesis postulates that the formation of lasting memories relies on at least two processes: the setting of a learning tag and the synthesis of plasticity related proteins, which once captured at tagged sites allow memory consolidation. BT explains how weak events, only capable of inducing transient forms of memories, can result in lasting memories when occurring close in time with other behaviorally relevant experiences that provide proteins. In this review, we detail the findings supporting the existence of BT process in rodents, leading to the consolidation, persistence, and interference of a memory. We focus on the molecular machinery taking place in these processes and describe the experimental data supporting the BT in humans.

No MeSH data available.


Strategies used to study the processes related to the setting of the learning tag and the PRPs synthesis in BT models. Weak training induces short- but not long-term memory and sets a leaning tag (dashed circle). The strong experience or different drugs (dopaminergic and adrenergic agonists) induces the synthesis of PRPs (red circle) that can be used to allow memory consolidation for a weak learning (green path). The local infusion of different inhibitory drugs (i.e., αCAMKII, PKA inhibitors, PKMζ blocker, or NMDA receptor antagonist) in brain structures close to the weak training can interfere with the proper setting and/or maintenance of the learning tag, impairing the promotion of LTM (red path). The local infusion of different drugs (i.e., protein synthesis inhibitors, antisense oligonucleotides, or D1/D5-dopaminergic, b-adrenergic, and NMDA receptors antagonists) in the target structure at the moment of PRPs synthesis also impaired the promotion of LTM (red path). Kinase activity requirement of TrkB receptor for both processes has been shown using Knock-in mice (see [43, 46, 54, 63, 64, 89]).
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fig4: Strategies used to study the processes related to the setting of the learning tag and the PRPs synthesis in BT models. Weak training induces short- but not long-term memory and sets a leaning tag (dashed circle). The strong experience or different drugs (dopaminergic and adrenergic agonists) induces the synthesis of PRPs (red circle) that can be used to allow memory consolidation for a weak learning (green path). The local infusion of different inhibitory drugs (i.e., αCAMKII, PKA inhibitors, PKMζ blocker, or NMDA receptor antagonist) in brain structures close to the weak training can interfere with the proper setting and/or maintenance of the learning tag, impairing the promotion of LTM (red path). The local infusion of different drugs (i.e., protein synthesis inhibitors, antisense oligonucleotides, or D1/D5-dopaminergic, b-adrenergic, and NMDA receptors antagonists) in the target structure at the moment of PRPs synthesis also impaired the promotion of LTM (red path). Kinase activity requirement of TrkB receptor for both processes has been shown using Knock-in mice (see [43, 46, 54, 63, 64, 89]).

Mentions: In sum, up to now the processes leading to the synthesis of PRPs seem to rely on dopaminergic and adrenergic systems, as well as on the requirement of NMDA receptors, with Arc and TrkB being two of the possible PRPs to be captured. On the other site the setting of the learning tag has been shown to be independent of PRPs synthesis and relying on NMDA receptors functionality as well as αCAMKII, PKA, PKMz, and TrkB. Most of these mechanisms that were reported using the IA-novel OF BT model but confirmed in schemas and WM spatial memory tasks are summarized in Figure 4. BT machinery has also been shown to be coincident with the mechanisms reported in the STC process for LTP. Nevertheless, a remarkable difference has been shown for the CFC-tag of extinction, which seems to rely on protein synthesis and to be independent of CAMKII activity.


Behavioral Tagging: A Translation of the Synaptic Tagging and Capture Hypothesis.

Moncada D, Ballarini F, Viola H - Neural Plast. (2015)

Strategies used to study the processes related to the setting of the learning tag and the PRPs synthesis in BT models. Weak training induces short- but not long-term memory and sets a leaning tag (dashed circle). The strong experience or different drugs (dopaminergic and adrenergic agonists) induces the synthesis of PRPs (red circle) that can be used to allow memory consolidation for a weak learning (green path). The local infusion of different inhibitory drugs (i.e., αCAMKII, PKA inhibitors, PKMζ blocker, or NMDA receptor antagonist) in brain structures close to the weak training can interfere with the proper setting and/or maintenance of the learning tag, impairing the promotion of LTM (red path). The local infusion of different drugs (i.e., protein synthesis inhibitors, antisense oligonucleotides, or D1/D5-dopaminergic, b-adrenergic, and NMDA receptors antagonists) in the target structure at the moment of PRPs synthesis also impaired the promotion of LTM (red path). Kinase activity requirement of TrkB receptor for both processes has been shown using Knock-in mice (see [43, 46, 54, 63, 64, 89]).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4562088&req=5

fig4: Strategies used to study the processes related to the setting of the learning tag and the PRPs synthesis in BT models. Weak training induces short- but not long-term memory and sets a leaning tag (dashed circle). The strong experience or different drugs (dopaminergic and adrenergic agonists) induces the synthesis of PRPs (red circle) that can be used to allow memory consolidation for a weak learning (green path). The local infusion of different inhibitory drugs (i.e., αCAMKII, PKA inhibitors, PKMζ blocker, or NMDA receptor antagonist) in brain structures close to the weak training can interfere with the proper setting and/or maintenance of the learning tag, impairing the promotion of LTM (red path). The local infusion of different drugs (i.e., protein synthesis inhibitors, antisense oligonucleotides, or D1/D5-dopaminergic, b-adrenergic, and NMDA receptors antagonists) in the target structure at the moment of PRPs synthesis also impaired the promotion of LTM (red path). Kinase activity requirement of TrkB receptor for both processes has been shown using Knock-in mice (see [43, 46, 54, 63, 64, 89]).
Mentions: In sum, up to now the processes leading to the synthesis of PRPs seem to rely on dopaminergic and adrenergic systems, as well as on the requirement of NMDA receptors, with Arc and TrkB being two of the possible PRPs to be captured. On the other site the setting of the learning tag has been shown to be independent of PRPs synthesis and relying on NMDA receptors functionality as well as αCAMKII, PKA, PKMz, and TrkB. Most of these mechanisms that were reported using the IA-novel OF BT model but confirmed in schemas and WM spatial memory tasks are summarized in Figure 4. BT machinery has also been shown to be coincident with the mechanisms reported in the STC process for LTP. Nevertheless, a remarkable difference has been shown for the CFC-tag of extinction, which seems to rely on protein synthesis and to be independent of CAMKII activity.

Bottom Line: BT explains how weak events, only capable of inducing transient forms of memories, can result in lasting memories when occurring close in time with other behaviorally relevant experiences that provide proteins.In this review, we detail the findings supporting the existence of BT process in rodents, leading to the consolidation, persistence, and interference of a memory.We focus on the molecular machinery taking place in these processes and describe the experimental data supporting the BT in humans.

View Article: PubMed Central - PubMed

Affiliation: Instituto de Biologia Celular y Neurociencias "Dr. Eduardo De Robertis", Facultad de Medicina, Universidad de Buenos Aires, C1121ABG Buenos Aires, Argentina.

ABSTRACT
Similar molecular machinery is activated in neurons following an electrical stimulus that induces synaptic changes and after learning sessions that trigger memory formation. Then, to achieve perdurability of these processes protein synthesis is required for the reinforcement of the changes induced in the network. The synaptic tagging and capture theory provided a strong framework to explain synaptic specificity and persistence of electrophysiological induced plastic changes. Ten years later, the behavioral tagging hypothesis (BT) made use of the same argument, applying it to learning and memory models. The hypothesis postulates that the formation of lasting memories relies on at least two processes: the setting of a learning tag and the synthesis of plasticity related proteins, which once captured at tagged sites allow memory consolidation. BT explains how weak events, only capable of inducing transient forms of memories, can result in lasting memories when occurring close in time with other behaviorally relevant experiences that provide proteins. In this review, we detail the findings supporting the existence of BT process in rodents, leading to the consolidation, persistence, and interference of a memory. We focus on the molecular machinery taking place in these processes and describe the experimental data supporting the BT in humans.

No MeSH data available.